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Objective:To explore the expression of calcium-binding protein 39 (CAB39) and vascular endothelial growth factor (VEGF) in bladder cancer tissues and their relationship with the prognosis of patients.Methods:A case-control study was conducted to select the focal tissues (case group) and post-operative paracancourous tissues (control group) from 94 bladder cancer patients who underwent surgery from Zibo Central Hospital from June 2014 to April 2018. Western blot and immunohistochemical staining were used to detect the expression of VEGF and CAB39 proteins in the two specimens. The positive expression rates of VEGF and CAB39 protein in bladder cancer tissues with different pathological characteristics were analyzed, and the relationship between VEGF and CAB39 protein expression and prognosis of patients with bladder cancer was analyzed by Cox proportional hazard regression model.Results:The relative expression levels of VEGF and CAB39 protein in the case group were significantly higher than those in the control group, with significant statistical difference (all P<0.05). The immunohistochemical staining scores of VEGF and CAB39 protein in the case group were higher than those in the control group, with statistically significant difference (all P<0.05). The positive expression rate of CAB39 protein was significantly higher in bladder cancer tissure of patients with low-grade, clinical stage T3-T4 and lymph node metastasis, with statistically significant difference (all P<0.05). The positive expression rate of VEGF protein was significantly higher in bladder cancer tissue of patients with clinical stage T3-T4 and lymph node metastasis, with statistically significant difference (all P<0.05). Cox proportional hazard regression model showed that low grade, clinical stage T3-T4, lymph node metastasis, positive expression of VEGF and CAB39 protein were independent risk factors for poor prognosis in bladder cancer patients in 3 years (all P<0.05). Conclusions:VEGF and CAB39 proteins are highly expressed in bladder cancer tissue, and have a certain relationship with the poor prognosis of patients.
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Epilepsy is a common neurological disorder characterized by hyperexcitability in the brain. Its pathogenesis is classically associated with an imbalance of excitatory and inhibitory neurons. Calretinin (CR) is one of the three major types of calcium-binding proteins present in inhibitory GABAergic neurons. The functions of CR and its role in neural excitability are still unknown. Recent data suggest that CR neurons have diverse neurotransmitters, morphologies, distributions, and functions in different brain regions across various species. Notably, CR neurons in the hippocampus, amygdala, neocortex, and thalamus are extremely susceptible to excitotoxicity in the epileptic brain, but the causal relationship is unknown. In this review, we focus on the heterogeneous functions of CR neurons in different brain regions and their relationship with neural excitability and epilepsy. Importantly, we provide perspectives on future investigations of the role of CR neurons in epilepsy.
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Humans , Amygdala/metabolism , Calbindin 2/metabolism , Epilepsy , GABAergic Neurons , Hippocampus/metabolismABSTRACT
Objective: to determine the presence and distribution of markers of the epithelialmesenchymal transition (EMT) (S-100A4 and alpha-smooth muscle actin-α-SMA) in gingival tissues of patients affected by Gingival hypertrophy (GH) due to orthodontics.GH is an exaggerated increase in gingival tissue whose pathogenesis is unknown. However, it has been reported that the epithelial-mesenchymal transition as a process involved in other types of GH. Materials and methods: descriptive study that included the analysis of gingival tissues of healthy individuals (n = 6) and patients with GH by orthodontic treatment (n = 6). Before gingival surgery, the patients underwent a periodontal hygiene phase. The gingival tissue samples obtained were processed and embedded in paraffin. The cuts were made with a microtome and deposited on polysine adhesion slides. Histological hematoxylin-eosin staining was performed.The identification and location of S-100A4 and α-SMA markers was determined by immunohistochemistry with monoclonal antibodies. The reading of the findings was carried out by oral pathologists. Results: in healthy individuals, an S100A4 label was observed in Langerhans cells, while α-SMA was identified in the vascular endothelium of all samples analysed. However, in patients with GH due to orthodontics, they registered an intense staining of S100A4 in gingival fibroblasts, Langerhans cells, vascular endothelium, and areas adjacent to the rupture of blood vessel. α-SMA expression in GO was detected in the vascular endothelium and gingival fibroblasts. Conclusion: the differential immunostaining of EMT markers in gingival tissues of patients with orthodontic GH suggests an eventual role of EMT in the pathogenesis of this pathology..Au
Objective: to determine the presence and distribution of markers of the epithelialmesenchymal transition (EMT) (S-100A4 and alpha-smooth muscle actin-α-SMA) in gingival tissues of patients affected by Gingival hypertrophy (GH) due to orthodontics. GH is an exaggerated increase in gingival tissue whose pathogenesis is unknown. However, it has been reported that the epithelial-mesenchymal transition as a process involved in other types of GH. Materials and methods: descriptive study that included the analysis of gingival tissues of healthy individuals (n = 6) and patients with GH by orthodontic treatment (n = 6). Before gingival surgery, the patients underwent a periodontal hygiene phase. The gingival tissue samples obtained were processed and embedded in paraffin. The cuts were made with a microtome and deposited on polysine adhesion slides. Histological hematoxylin-eosin staining was performed. The identification and location of S-100A4 and α-SMA markers was determined by immunohistochemistry with monoclonal antibodies. The reading of the findings was carried out by oral pathologists. Results: in healthy individuals, an S100A4 label was observed in Langerhans cells, while α-SMA was identified in the vascular endothelium of all samples analysed. However, in patients with GH due to orthodontics, they registered an intense staining of S100A4 in gingival fibroblasts, Langerhans cells, vascular endothelium, and areas adjacent to the rupture of blood vessel. α-SMA expression in GO was detected in the vascular endothelium and gingival fibroblasts. Conclusion: the differential immunostaining of EMT markers in gingival tissues of patients with orthodontic GH suggests an eventual role of EMT in the pathogenesis of this pathology..Au
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Humans , Patients , Tissues , S100 Calcium-Binding Protein A4ABSTRACT
Objective To investigate the effect of propofol on cognitive function in young obese rats, and to explore its relationship with heme oxygenase 1 (HO-1), superoxide dismutase 1 (SOD1) protein expression and plasma S100 calciumbinding protein β (S100β) expression. Methods A total of 140 male SD rats aged 21 days were randomly divided into normal diet group (n=40) and high-fat diet group (n=100), and the rats were fed with a normal diet and a high-fat diet, respectively. After 4 weeks of feeding, 40 rats of the high-fat diet group with body mass≥the average body mass ≥1.4 times of the standard deviation of the normal diet group were designated as obese rats. The rats in the normal diet group were randomly divided into the normal lipid emulsion solvent group (NL group) and the normal propofol group (NP group), and the 40 obese rats were randomly divided into the obese lipid emulsion solvent group (OL group) and the obese propofol group (OP group), with 20 rats in each group. The rats in the propofol groups were intraperitoneally given propofol 100 mg/kg, and those in the lipid emulsion solvent groups (control groups) were intraperitoneally given lipid emulsion solvent 100 mg/kg, once a day for 7 days. On the first day after drug withdrawal, Morris water maze test was performed to evaluate the spatial learning and memory abilities of rats in each group. Meanwhile, the plasma S100β protein content of each group was detected by enzyme-linked immunosorbent assay, the expression levels of HO-1 and SOD1 protein in hippocampus were detected by Western blotting, and the changes of neurons in hippocampus CA1 area were observed by hematoxylin-eosin staining. Results Compared with the OL group, the escape latency time was significantly prolonged on 1-5 days (all P0.05). Conclusion Propofol can down-regulate the expression of anti-oxidant factors HO-1 and SOD1 in the hippocampus of young obese rats, leading to increase of S100β expression and oxidative stress and eventually causing cognitive impairment..
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Objective::To explore the effect of Zuoguiwan on the bone mineral density (BMD) and the expressions of Ca2+ transport-associated protein in ovariectomized rats. Method::The 48 female SD rats were randomly divided into six groups: normal group, model group, sham operation group, estrogen group(0.167 mg·kg-1) and low and high-dose Zuoguiwan groups(9.6, 38.4 g·kg-1), with 10 rats in each group. Except for the sham-operated group, the ovariectomized rats in the other groups received the bilateral ovariectomy. Therapeutic intervention was given in each group for 3 months after the establishment of the model. After 12 weeks, BMD was measured using dualenergy X-ray absorptiometry. Tartrated presistant acid phosphatse(TRACP) and serum calcium were detected by biochemical kits.Protein expression in Ca2+ transport (Bone tissue) was detected by Western blot. Result::Compared with the normal group, the serum calcium of the model group was decreased(P<0.01). Compared with the normal group, BMD of the model group was decreased (P<0.01). The serum calcium of rats in high-dose group and western medicine group was higher than that of model group(P<0.01). BMD in model group was lower than that of Zuoguiwan groups and estrogen group(P<0.05). There was no significant difference in TRACP among the groups. Nilestriol and Zuoguiwan can down-regulate the expressions of TRPV5, NCX1, CaBP-D28K and PMCA1b in bone tissue of castrated rats(P<0.05, P<0.01). Conclusion::Zuoguiwan can down-regulate the expressions of Ca2+ transport-associated proteins (Bone tissues) in rat osteoclasts, with an efficacy on osteoporosis.
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PURPOSE: To explore the influence of S100 calcium binding protein A4 (S100A4) knockout (KO) on methionine-choline-deficient (MCD) diet-induced non-alcoholic fatty liver disease (NAFLD) in mice. MATERIALS AND METHODS: S100A4 KO mice (n=20) and their wild-type (WT) counterparts (n=20) were randomly divided into KO/MCD, Ko/methionine-choline-sufficient (MCS), WT/MCD, and WT/MCS groups. After 8 weeks of feeding, blood lipid and liver function-related indexes were measured. HE, Oil Red O, and Masson stainings were used to observe the changes of liver histopathology. Additionally, expressions of S100A4 and proinflammatory and profibrogenic cytokines were detected by qRT-PCR and Western blot, while hepatocyte apoptosis was revealed by TUNEL staining. RESULTS: Serum levels of aminotransferase, aspartate aminotransferase, triglyceride, and total cholesterol in mice were increased after 8-week MCD feeding, and hepatocytes performed varying balloon-like changes with increased inflammatory cell infiltration and collagen fibers; however, these effects were improved in mice of KO/MCD group. Meanwhile, total NAFLD activity scores and fibrosis were lower compared to WT+MCD group. Compared to WT/MCS group, S100A4 expression in liver tissue of WT/MCD group was enhanced. The expression of proinflammatory (TNF-α, IL-1β, IL-6) and profibrogenic cytokines (TGF-β1, COL1A1, α-SMA) in MCD-induced NAFLD mice were increased, as well as apoptotic index (AI). For MCD group, the expressions of proinflammatory and profibrogenic cytokines and AI in KO mice were lower than those of WT mice. CONCLUSION: S100A4 was detected to be upregulated in NAFLD, while S100A4 KO alleviated liver fibrosis and inflammation, in addition to inhibiting hepatocyte apoptosis.
Subject(s)
Animals , Mice , Apoptosis , Aspartate Aminotransferases , Blotting, Western , Calcium , Carrier Proteins , Cholesterol , Collagen , Cytokines , Fibrosis , Hepatocytes , In Situ Nick-End Labeling , Inflammation , Liver , Liver Cirrhosis , Non-alcoholic Fatty Liver Disease , TriglyceridesABSTRACT
Objective To elucidate the impact of over-expression of S100A7 on migration,invasion,proliferation, cell cycle, and epithelial-mesenchymal transition (EMT) in human cervical cancer HeLa and CaSki cells.Methods(1)Immunohistochemistry of SP was used to examine the expression of S100A7 in 40 cases of squamous cervical cancer tissues and 20 cases of normal cervical tissues.(2)The vectors of pLVX-IRES-Neo-S100A7 and pLVX-IRES-Neo were used to transfect human cervical cancer HeLa and CaSki cells, and the positive clones were screened and identified. Next, transwell migration assay, cell counting kit-8(CCK-8)assay and fluorescence activating cell sorter(FACS)were used to detect the effect of S100A7-overexpression on the migration, invasion, proliferation and cell cycle of cervical cancer cells. Furthermore, western blot was performed to observe the expression of epithelial marker(E-cadherin)and mesenchymal markers(N-cadherin,vimentin,and fibronectin)of EMT. Results(1)S100A7 expression was significantly higher in cervical squamous cancer tissues(median 91.6)than that in normal cervical tissues(median 52.1;Z=-2.948,P=0.003).(2)Stable S100A7-overexpressed cells were established using lentiviral-mediated gene delivery in HeLa and CaSki cells. S100A7 was detected by real-time quantitative reverse transcription PCR,S100A7 mRNA of S100A7-overexpressed cells were 119 ± 3 and 177 ± 16, increased significantly compared with control groups of median(P<0.01).Compared with the control cells, the number of S100A7-overexpressed HeLa and CaSki cells that passed the transwell membrane assay were increased significanatly(572 ± 51 vs 337 ± 25, P<0.01;100 ± 8 vs 41 ± 4, P<0.01).Matrigel invasion assay showed that the number of S100A7-overexpressed HeLa and CaSki cells that passed the transwell membrane were respectively 441±15 and 110±14,elevated significantly compared with control cells(156±21 and 59±7;P<0.05). However, S100A7 overexpression didn′t influence the proliferation and cell cycle progression of HeLa and CaSki cells(P>0.05). Expression of E-cadherin was dramatically decreased, while N-cadherin, vimentin, and fibronectin increased in S100A7-overexpressed cells. Conclusion S100A7 enhances the migration, invasion and EMT of HeLa cells and CaSki cells, and may be plays an important role in the development of cervical cancer.
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Objective To investigate the mechanism of inducing production of vascular endothelial growth factors (VEGF) by recombinant human S100 calcium binding protein A4 (rhS100A4) in rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs).Methods Synovial tissue was sampled from the patients with rheumatoid arthritis (RA) undergoing knee arthroplasty for in vitro culture of RAFLSs.CCK-8 assay was conducted to detect the effect of rhS100A4 and the effect of its interaction with Rapamycin (Rap),an inhibitor of mammalian rapamycin target 1 (mTORC1) signaling pathway,on the proliferation of RAFLSs.The effects of rhS100A4 and its interaction with Rap on the expression of VEGF in RAFLSs were detected by immunofluorescence.After rhS100A4 and its cooperation with Rap stimulated the conditioned medium (CM)produced by RAFLSs,the effect of CM on formation of lumen in human unbilical vein endothelial cells (HUVECs) in vitro was observed to detect the angiogenic ability of rhS100A4.Western blot was used to detect the effect of rhS100A4 on the phosphorylation of downstream ribosomal protein S6 (S6) in the mTORC1 signaling pathway in RAFLSs and to analyze the effects of rhS100A4 and Rap on phosphorylation of S6 protein and expression of VEGF protein in RAFLSs.Results rhS100A4 promoted cell proliferation and expression of VEGF protein in RAFLSs,and the CM formed by rhS100A4 promoted HUVECs to form blood vessels in vitro.Rap inhibited the above biological effects of rhS100A4,rhS100A4 activated the downstream protein S6 in the mTORC1 signaling pathway in RAFLSs cells to increase their phosphorylation levels.The effects of rhS100A4 on the phosphorylation of S6 protein and on the expression of VEGF protein in RAFLSs were inhibited by Rap.Conclusion rhS10OA4 promotes production of VEGF in RAFLSs by activating the mTORC 1 signaling pathway.
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Objective To investigate the changes of brain edma and expression of blood high mobil-ity group box 1(HMGB1) and calcium binding protein S100B after traumatic brain injury (TBI) in IL-4 knockout (IL-4 KO) mice,and to explore the effects of IL-4 on traumatic brain injury. Methods Twenty male wild type ( WT) or twenty male IL-4 KO BALB/cJ mice were randomly divided into WT sham TBI group,WT TBI group,IL-4 KO sham TBI group and IL-4 KO TBI group(n=10 in each group).The model of traumatic brain injury was established by the free falling body epidural impact method,then the brain water content was measured. The expression of aquaporin-4 ( APQ4) and HMGB1 in injured brain of each group was detected by Western blot,and the concentration of HMGB1 and S100B in serum was detected by ELISA assay. Results ( 1 ) The brain water content of injured lateral brain of BALB/cJ mice with IL-4 gene knockout was significantly higher than that of wild type mice with brain injury model (WT group: (80.03± 0.35)％;IL-4 KO group:(81.93±0.41)％;P<0.05).(2) The Western blot showed that the expression of AQP4 and HMGB1 in brain tissue of BALB/cJ mice with IL-4 gene knockout was significantly higher than those in wild type mice after traumatic brain injury. ( 3) The results of ELISA showed that the levels of HMGB1 and S100B in the serum of IL-4 knockout BALB/cJ mice were significantly higher than those of wild type mice (HMGB1:WT group:(9.21±0.74)ng/ml;IL-4 gene knock-out group:(13.39±1.33)ng/ml,P<0.05;S100B protein:WT group:(11.11±0.84)pg/ml;IL-4 KO group: (18.11±2.02)pg/ml,P<0.05 ). Conclusion The brain tissue water content and the expression of APQ4 are increased in IL-4 KO TBI mice.The expression of HMGB1 in brain issue and serum and S100B in serum are also up-regulated.
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Objective To observe the effect of ossotide injection on bone mineral density (BMD), bone microstructure and biomechanical properties and mRNA expression of small intestinal calcium binding protein (CaBp-D9K), and to study the mechanism of ossotide injection in the treatment of ovariectomized osteoporosis. Methods Forty-eight 3-month old SPF male rats with successful modeling (excision of bilateral ovaries) were randomly divided into the observation group and model group, 24 normal rats were divided into sham operation group (excised part of the mesenteric membrane), and 24 normal blank group. The blank group, sham operation group and model group were given normal saline, and the observation group was intragastrically given 1. 1 mg/kg ossotide. Two months after intervention, the bone volume (BV), trabecular bone volume (Tb. Th), trabecular number (Tb. N), trabecular separation (Tb. Sp), bone mineral density, bone biomechanics, serum 1,25(OH)2D3 levels and CaBp-D9K mRNA expression levels of small intestine were assessed and statistically analyzed. Results The bone mineral density, maximum load, fracture load, BV, Tb. Th, Tb. N, serum 1, 25 (OH ) 2D3 and intestinal CaBp-D9K mRNA expression level in the model group were significantly lower than those of the control group and sham operation group (P＜ 0. 05), Tb. Sp of the model group was significantly higher than that of the control group and sham operation group (P ＜ 0. 05 ). The bone mineral density, maximum load, fracture load, BV, Tb. Th, Tb. N, serum 1,25(OH)2D3 and intestinal CaBp-D9K mRNA expression level in the observation group were significantly higher than those of the model operation group, and the Tb. Sp of the observation group was lower than that of the model group (P ＜ 0. 05). Conclusions Ossotide injection treatment can reduce the degree of osteoporosis in ovariectomized rats, increasing intestinal CaBp-D9k mRNA expression and promoting intestinal calcium absorption may be its important mechanisms of action.
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Objective To investigate the diagnostic value of cranial ultrasonic examination combined with the detection of serum neuron specific enolase(NSE),S100B and interleukin-6(IL-6)on cerebral white matter lesions of premature infant. Methods Thirty-nine premature infants with cerebral white matter injury diagnosed by cranial magnetic resonance imaging (MRI)in Women and Infants Hospital of Zhengzhou City from August 2016 to July 2017 were selected as observation group. Another thirty premature infants without brain white matter injury were selected as control group in the same period. On the 1st , 3rd and 7th day after birth,the serum NSE level was detected by the automatic time resolved fluoroimmunoassay system,the lev-els of serum S100B and IL-6 were detected by double anti sandwich enzyme-linked immunosorbent assay,and the changes of the cerebral white matter echoes around the cerebral ventricles were observed by cranial ultrasonic examination. The sensitivi-ty,specificity and accuracy combined detection of cranial ultrasonic examination combined with serum NSE,S100B and IL-6 in the diagnosis of white matter lesions in premature infants were analyzed. Results The detection rate of cerebral white matter lesions by cranial ultrasonic examination in the control group was 6. 45％(2 / 31),3. 23％(1 / 31)and 0. 00％(0 / 31)respec-tively;and it was 92. 31％(36 / 39),87. 18％(34 / 39)and 84. 62％(33 / 39)respectively on the 1st ,3rd and 7th day after birth in the observation group;the detection rate of cerebral white matter lesions in the observation group was significantly higher than that in the control group on the 1st ,3rd and 7th day after birth(χ2 = 51. 30,48. 69,49. 63;P < 0. 05). There was no signifi-cant difference in the grayscale value of cerebral white matter among the 1st ,3rd and 7th day after birth in the two groups(P >0. 05). The grayscale value of cerebral white matter in the observation group was significantly higher than that in the control group on the 1st ,3rd and 7th day after birth(P < 0. 05). There was no significant difference in serum S100B and IL-6 levels a-mong the 1st ,3rd and 7th day after birth in the control group(F = 0. 319,0. 307;P > 0. 05). There was the significant difference in serum NSE level among the 1st ,3rd and 7th day after birth in the control group(F = 3. 298,P < 0. 05),the serum NSE level on the 3rd and 7th day after birth was significantly lower than that on the 1st day after birth(P < 0. 05),the serum NSE level on the 7th day after birth was significantly lower than that on the 3rd day after birth(P < 0. 05). The levels of serum NSE,S100B and IL-6 in the observation group showed the downward trend on the 1st ,3rd and 7th day after birth(F = 3. 323,3. 517,3. 706;P < 0. 05). The levels of serum NSE,S100B and IL-6 on the 3rd and 7th day after birth were significantly lower than those on the 1st day after birth in the observation group(P < 0. 05). There was no significant difference in the levels of serum NSE, S100B and IL-6 between the 3rd and 7th day after birth in the observation group(P < 0. 05). The levels of serum NSE,S100B and IL-6 in the observation group were significantly higher than those in the control group on the 1st ,3rd and 7th day after birth (P < 0. 05). In the observation group,the grayscale value of cerebral white matter was positively correlated with the levels of serum NSE,S100B and IL-6 on the 1st day after birth(r = 3. 137,3. 358,3. 056;P < 0. 05);the grayscale value of cerebral white matter was positively correlated with the levels of serum NSE and S100B on the 3rd day after birth(r = 2. 872,2. 347;P <0. 05);the grayscale value of cerebral white matter was positively correlated with serum S100B level on the 7th day after birth (r = 2. 791,P < 0. 05). The sensitivity,specificity and accuracy of combined detection of cranial ultrasonic examination and, serum NSE and S100B in the diagnosis of cerebral white matter lesions in premature infants was 100. 00％,93. 54％ and 97. 14％ respectively. Conclusion The combined detection of cranial ultrasonic examination,serum NSE and S100B can sig-nificantly improve the accuracy of early diagnosis of cerebral white matter lesions.
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The expression of calcium binding protein S100A8 in 30 controls of normal oral tissue and 35 cases of OSCC was detected by immunohistochemical staining and Western blot respectively. The positive expression of S100A8 protein in OSCC and the controls was 68. 5％ and 36. 7％ respectively(P ＜ 0. 05). S100A8 may play a role in the development of OSCC.
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Cerebrospinal fluid and level of blood S100B protein are significantly higher in patients with intracerebral hemorrhage,which are associated the differentiation of stroke,damage of blood-brain barrier,hematoma volume,brain edema,degree of nerve function defect,and outcomes.Therefore,S100B is expected to be used in the diagnosis of intracerebral hemorrhage,assessment of injury and outcomes,and even as a biomarker of therapeutic targets.
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The histidine enriched calcium protein (HRC)is a new type of sarcoplasmic reticulum (SR) regulator of Ca2 + absorption,storage and release,located in the lumen cavity,with a combination of high capacity and low affinity of calcium ions.Recent studies have shown that abnormal expression of HRC plays a key role in the development of hepatocellular carcinoma.This article reviews the role of HRC in hepatocellular carcinoma.
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Objective: To investigate the role and mechanism of S100 calcium binding protein B (S100B) in osteoarthritis (OA) cartilage damage repair. Methods: Twenty New Zealand rabbits were randomly divided into control group and model group, with 10 rabbits in each group. Rabbits in the model group were injured by the right knee joint immobilization method to make the artilage injury model, while the control group did not deal with any injury. After 4 weeks, the levels of interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) in synovial fluid were detected by ELISA method; the mRNA and protein expressions of S100B, fibroblast growth factor 2 (FGF-2), and FGF receptor 1 (FGFR1) in cartilage tissue were examined by real-time fluorescence quantitative PCR (qRT-PCR) and Western blot assay. Human synovial fibroblasts (SF) were isolated and cultured in vitro. The effects of S100B overexpression and knockdown on the levels of IL-1β and TNF-α (ELISA method) and the expressions of FGF-2 and FGFR1 gene (qRT-PCR) and protein (Western blot) were observed. Moreover, the effects of FGFR1 knockdown in above S100 overexpression system on the levels of IL-1β and TNF-α (ELISA method) and the expressions of FGF-2 and FGFR1 gene (qRT-PCR) and protein (Western blot) were observed. Results: ELISA detection showed that the expressions of IL-1β and TNF-α in the synovial fluid of the model group were significantly higher than those of the control group ( P<0.05); qRT-PCR and Western blot detection showed that the mRNA and protein expressions of S100B, FGF-2, and FGFR1 in cartilage tissue were significantly higher than those of the control group ( P<0.05). Overexpression and knockdown S100 could respectively significantly increase and decrease lipopolysaccharides (LPS) induced IL-1β and TNF-α levels elevation and the mRNA and protein expressions of FGF-2 and FGFR1 ( P<0.05); whereas FGFR1 knockdown could significantly decrease LPS induced IL-1β and TNF-α levels elevation and the mRNA and protein expressions of FGF-2 and FGFR1 ( P<0.05). Conclusion: S100B protein can regulate the inflammatory response of SF and may affect the repair of cartilage damage in OA, and the mechanism may be related to the activation of FGF-2/FGFR1 signaling pathway.
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Objective To analyze the relationship between the level of serum calcium binding protein S 100A12 and the severity of acute pancreatitis (AP) ,so as to provide a simple and reliable method for judging the severity of AP .Methods A total of 68 pa-tients with AP from January 2015 to January 2016 in Luzhou Hospital of Traditional Chinese Medicine were selected as objects in this study ,and complete the examination after diagnosis ,modified CT severity index (MCTSI) was used to grade the severity ,serum calcium binding protein S100A12were tested and compared in patients with different disease grading .The ROC curve of different se-verity patients were made .Judging the severity of critical value according to the S 100A12 curve inflection point ,basing on the judg-ment of MCTSI ,the sensitivity ,specificity and accuracy of S 100A12 in grading condition of AP were calculated ,then the value of S100A12 was evaluated .Results The level of S100A12 increased with MCTSI grade rising ,there were significant differences in S100A12 level between different grades patients(P<0 .05) .ROC curve analysis showed that the clinical limits of gradeⅠto Ⅲ were 26-80 ,81-260 ,>260 ng/mL respectively .The sensitivities accuracy of S100A12 judging grade Ⅰ ,grade Ⅱ and grade Ⅲ were 88 .89% ,94 .12% ,80 .00% ,the specificity were 75 .00% ,94 .12% ,96 .55% ,the accuracy were 82 .35% ,94 .12% ,94 .12% respec-tively .Conclusion The serum calcium binding protein S100A12 estimates is consistent with MCTSI for judging the severity condi-tion of AP .
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Objective To analyze the relationship between the level of serum calcium binding protein S 100A12 and the severity of acute pancreatitis (AP) ,so as to provide a simple and reliable method for judging the severity of AP .Methods A total of 68 pa-tients with AP from January 2015 to January 2016 in Luzhou Hospital of Traditional Chinese Medicine were selected as objects in this study ,and complete the examination after diagnosis ,modified CT severity index (MCTSI) was used to grade the severity ,serum calcium binding protein S100A12were tested and compared in patients with different disease grading .The ROC curve of different se-verity patients were made .Judging the severity of critical value according to the S 100A12 curve inflection point ,basing on the judg-ment of MCTSI ,the sensitivity ,specificity and accuracy of S 100A12 in grading condition of AP were calculated ,then the value of S100A12 was evaluated .Results The level of S100A12 increased with MCTSI grade rising ,there were significant differences in S100A12 level between different grades patients(P<0 .05) .ROC curve analysis showed that the clinical limits of gradeⅠto Ⅲ were 26-80 ,81-260 ,>260 ng/mL respectively .The sensitivities accuracy of S100A12 judging grade Ⅰ ,grade Ⅱ and grade Ⅲ were 88 .89% ,94 .12% ,80 .00% ,the specificity were 75 .00% ,94 .12% ,96 .55% ,the accuracy were 82 .35% ,94 .12% ,94 .12% respec-tively .Conclusion The serum calcium binding protein S100A12 estimates is consistent with MCTSI for judging the severity condi-tion of AP .
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AIM:To study the expression level of S100 calcium-binding protein A4 (S100A4) in synovial tissue of the knee joint in rheumatoid arthritis (RA) patients and normal persons, and the effect of S100A4 on the angiogenesis induced by rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs).METHODS:The synovial tissue was taken from the knee joint of the RA patients (RA group) and the normal persons (control group).The protein expression of S100A4 and vascular endothelial growth factor (VEGF) in the synovial tissue of the 2 groups was observed by immunohistochemistry.RAFLSs were isolated from synovial tissue of patients with active RA.ELISA was used to detect the effect of S100A4 on the secretion of VEGF by RAFLSs.The effect of S100A4 on the angiogenesis of HUVECs cultured with conditioned medium from RAFLSs was also detected.RESULTS:The protein of S100A4 and VEGF was highly expressed in the synovial tissues of RA group (P<0.05).rhS100A4 significantly stimulated the secretion of VEGF in RAFLSs in a time-and dose-dependent manner (P<0.05).Cultured with conditioned medium from RAFLSs, rhS100A4 significantly promoted HUVECs to form tube-like structures in vitro.CONCLUSION:S100A4 protein is highly expressed in synovial tissue of the knee joint in RA patients, and S100A4 stimulates synovial angiogenesis by promoting RAFLSs to generate VEGF, indicating that S100A4 may be used as a potential target for the treatment of RA.
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Objective To investigate the serum level of calcium-binding protein A9(S100A9)in patients with rheumatoid arthritis and explore its potential clinical significance. Methods The serum level of S100A9 was measured by ELISA in 79 rheumatoid arthritis (RA) patients and 20 healthy controls (HC). The correlation of S100A9 level and relevant clinical parameters were analyzed. Results The serum level of S100A9 was significantly increase in RA patients than those in HC. The serum level of S100A9 was higher in high disease activity than that in moderate and low disease activity in the RA group. There was a positive correlation in serum S100A9 level and DAS28 score,Rheumatoid factor,tender joint count and swollen joint count. Conclusion The serum level of S100A9 increases in RA patients and correlates with RA activity.
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Objective To evaluate the effect of metformin on inflammatory response around the hematoma after intracerebral hemorrhage (ICH) in mice. Methods A total of 60 male C57/BL6 mice were randomly divided into 3 groups:Sham group, model group and metformin group, 20 mice for each group. The model group and metformin group were injected bacterial collagenase (1 μL, 0.075 U) into the striatum. The Sham group was injected 1 μL saline into the striatum. The metformin group was treated with metformin (gavage administration, 100 mg/kg) 6 h after ICH and for 7 consecutive days. The model group was given equal saline orally. The expression levels of myeloperoxidase (MPO) and the calcium binding protein 1 (Iba-1) around the hematoma (microglia) were detected by immunohistochemical staining at 3 days and 7 days after ICH. Interleukin-1β and TNF-α were detected by Western blot assay at 3 days after ICH. Results Results of immunohistochemical staining showed that the positive expression levels of MPO and Iba-1 were significantly lower than those in model group 3 days and 7 days after treatment (P<0.05). The expression levels of IL-1β and TNF-α were significantly lower in metformin group than those in model group 3 days after treatment (P<0.05). Conclusion Metformin can reduce the infiltration of inflammatory cytokines and inflammatory cells and the excessive activation of microglia after ICH in mice.